Search Results (2,000)

Background: Continuous glucose monitoring (CGM) may overcome the limitations of intermittent point-of-care (POC) testing by providing real-time glucose trends and reducing treatment delays. This study aimed to evaluate the efficacy of CGM versus POC capillary testing in improving glycemic control among hospitalized non-Intensive Care Unit (non-ICU) adults with type 2 diabetes mellitus (T2DM). Methods: We conducted a systematic review and meta-analysis following PRISMA 2020 guidelines. We searched PubMed for randomized controlled trials published in English or Spanish that compared CGM with POC testing in hospitalized non-ICU adults ≥ 18 years old with T2DM and assessed risk of bias using the Cochrane RoB2 tool. The primary outcome was time in range (TIR). Secondary outcomes included time below range (TBR), time above range (TAR), mean glucose (MG), and glycemic variability (GV). Results: Seven randomized controlled trials (RCTs) including 1106 patients were analyzed. CGM significantly improved TIR (mean difference [MD] +8.15%; 95% confidence interval [CI]: +5.76, +10.55; p < 0.001) and reduced TAR > 180 mg/dL (MD −7.11%; 95% CI: −9.43, −4.78; p < 0.001) and TAR > 250 mg/dL (MD −3.96%; 95% CI: −5.29, −2.62; p < 0.001) compared with POC testing. MG also decreased with CGM (MD −11.27 mg/dL; 95% CI: −14.74, −7.81; p < 0.001). A modest reduction in TBR <70 mg/dL was observed (MD −0.29%; p < 0.001), whereas no significant differences were found for TBR < 54 mg/dL or GV. Conclusions: CGM improves inpatient glycemic control in non-ICU adults with type 2 diabetes, demonstrating advantages over POC testing across multiple randomized trials. However, further multicenter research is needed to clarify workflow implications, cost-effectiveness, and optimal implementation strategies. Full article

Background and Objectives: Peripheral arterial disease (PAD), frequently observed in individuals with type 2 diabetes mellitus (T2DM), is associated with diminished life quality, increased cardiovascular risk, and higher mortality rates. Similarly, trimethylamine N-oxide (TMAO), a uremic toxin produced by gut microbiota, has been linked to hypertension, cardiovascular disease, and increased overall mortality. In this study, we aimed to investigate whether serum TMAO levels are related to PAD in T2DM cases. Materials and Methods: In this cross-sectional investigation performed at one medical center, 120 patients with type 2 diabetes mellitus (T2DM) were included. High-performance liquid chromatography–mass spectrometry and an automated oscillometric device were used to measure serum TMAO levels and ankle–brachial index (ABI) values, respectively. Individuals exhibiting an ABI of less than 0.9 were classified as belonging to the low-ABI group. Results: Of the 120 participants, 23 (19.2%) had low ABI. Compared with the normal-ABI group, the low-ABI group was older (p = 0.017) and exhibited higher levels of urine albumin-to-creatinine ratio (UACR, p < 0.001), C-reactive protein (CRP, p < 0.001), and TMAO (p < 0.001). After adjusting for age, UACR, and CRP, multivariable logistic regression analysis identified serum TMAO concentration as an independent predictor of PAD in T2DM patients (odds ratio [OR]: 1.051; 95% confidence interval [CI]: 1.017–1.086; p = 0.003). In Spearman’s rank correlation analyses, log-transformed left ABI (log-left ABI, p = 0.017) and log-right ABI (p = 0.001) negatively correlated with log-TMAO. In patients with T2DM, the predictive performance of serum TMAO levels for PAD yielded an area under the receiver operating characteristic (ROC) curve of 0.812 (95% CI: 0.701–0.923; p < 0.001). Conclusions: Among individuals with T2DM, higher serum TMAO levels were associated with lower left and right ABI values and an increased likelihood of PAD. Full article

Diabetes mellitus (DM) is a complex, heterogeneous, hyperglycemic chronic metabolic disorder. Type 2 diabetes mellitus (T2DM) is characterized by progressive loss of insulin secretion from pancreatic islet β-cells due to IR (insulin resistance), which is a feature of metabolic syndrome (MetS). Chronic hyperglycemia in patients with T2DM in synergy with other metabolic abnormalities causes complications such as diabetic ketoacidosis, osmotic diuresis and hyperglycemic diabetic coma, as well as chronic microvascular and macrovascular complications such as atherosclerotic cardiovascular disease (ASCVD), peripheral artery disease (PAD) and cerebrovascular events, which implicate the formation of reactive species and the promotion of inflammatory pathways. In these events, natural or synthetic antioxidants and minerals seem to have ameliorative effects and may serve as beneficial co-treatment options. In view of these terms, the aim of this study is to investigate the underlying mechanisms of T2DM, its clinical presentation, and its complications. Additionally, the association of the pathogenesis of T2DM and the occurrence of its complications with obesity, chronic inflammation, oxidative stress (OS), insulin resistance (IR), hepatic steatosis, and dyslipidemia is examined, whilst molecular pathways, such as NF-κB and JAK/STAT, are also summarized, under the scope of the effects of several antioxidant compounds and minerals on their progression. The interrelation of T2DM with these conditions, as well as the effects of antioxidant supplementation, seems to be bidirectional, and it is recommended that obese patients be screened for T2DM and adopt lifestyle changes, including exercise, diet modification, and weight loss, in addition to potentially taking multifunctional supplements that offer antioxidant and anti-inflammatory potential. However, many aspects of the protective mechanisms of such antioxidants remain to be elucidated, with more drawbacks in their pharmacokinetic behavior, such as their poor absorption and solubility, waiting to be resolved. Full article

Chronic hyperglycemia inflicts serious cellular damage by inducing oxidative stress through the excessive production of free radicals. This oxidative milieu may impair the cellular redox capacity and disrupt the insulin-like growth factor (IGF) system, thereby increasing the risk of cardiovascular complications. This study aimed to investigate plasma levels of components of the IGF system and antioxidant biomarkers in young adults with type 1 diabetes mellitus (T1DM) compared to age-matched healthy controls in Brazil. This study included 129 patients with T1DM (76 female, 53 male; mean age 26.97 ± 0.6 years) and 95 healthy controls (61 female, 34 male; mean age 27.35 ± 0.68 years). Young Brazilian adults with T1DM had significantly lower mean IGF-I and higher mean IGFBP-1 levels compared to healthy controls. The T1DM group showed a more atherogenic profile, characterized by a significantly elevated ApoB/ApoA1 ratio and increased oxidized LDL levels. However, a subset of patients with significantly better glycemic control exhibited serum IGF-I and IGFBP-1 levels within the normal range observed in controls, which may indicate the presence of residual functional beta-cell activity or reflect better glycemic control in this subgroup. Antioxidant components and oxidative stress biomarkers were significantly upregulated in the T1DM group compared to the control group, suggesting a compensatory adaptive response. No significant correlation was observed between biomarkers of oxidative stress and the IGF-system. Full article

Background/Objective: Diabetic nephropathy (DN), a key microvascular complication of type 2 diabetes (T2DM), drives significant morbidity, mortality, and healthcare costs. Vitamin D deficiency has been linked to renal dysfunction, but its role in DN remains unclear. This study assessed the association between vitamin D status and DN versus T2DM without nephropathy. Methods: This cross-sectional hospital-based study included 399 participants (299 DN, 100 T2DM without nephropathy) at a tertiary endocrine clinic. Demographic, clinical, and biochemical data, including serum 25(OH)D, were collected. Chi-square and Mann–Whitney compared categorical and continuous variables, respectively, and multinomial logistic regression assessed the association between vitamin D status and DN (p < 0.05). Results: Patients with DN were older (58.2 ± 7.95 vs. 51.4 ± 9.94 years, p < 0.001), had more advanced CKD (stages 2–3b: 84.6% vs. 20.0%, p < 0.001), and higher albuminuria (moderate: 80.3% vs. 19.0%; severe: 18.4% vs. 0%, p < 0.001). They also showed poorer glycemic control, elevated urea and creatinine, lower serum albumin, dyslipidemia, elevated liver enzymes, and higher uric acid (all p < 0.05). Vitamin D deficiency was more prevalent in DN (37.7% vs. 8.0%, p < 0.001). Unadjusted multinomial regression indicated that T2DM patients without nephropathy had a 91% lower risk of vitamin D deficiency (RRR 0.09; 95% CI 0.04–0.19, p < 0.001) and an 87% lower risk of insufficiency (RRR 0.13; 95% CI 0.05–0.26, p < 0.001) compared with DN patients. After adjusting for age, HbA1c, creatinine, duration of diabetes and eGFR, the reduced risk of deficiency remained significant (RRR 0.04; 95% CI 0.01–0.16, p < 0.001), while the association with insufficiency was no longer significant (p = 0.310). Conclusions: This study shows a significant association between vitamin D deficiency and diabetic nephropathy, though its cross-sectional design precludes causal inference. Reverse causality and residual confounding cannot be excluded. Patients with DN had poorer glycemic control, dyslipidemia, and renal function, along with more frequent vitamin D deficiency. Routine vitamin D monitoring may support early detection and risk stratification in T2DM. Full article

Background: Patients with type 2 diabetes mellitus (T2DM) and inflammatory bowel disease (IBD) face elevated risk of hepatobiliary complications. The biliary safety of GLP-1 and dual GLP-1/GIP receptor agonists in this population is uncertain. Methods: We conducted a retrospective cohort study using the TrinetX LIVE global health research network. Adults (≥18 years) with coexisting T2DM and IBD were assigned to exposure (semaglutide or tirzepatide) or comparator (no GLP-1/GIP therapy) cohorts. The index was first prescription (or matched date). Primary outcomes—cholelithiasis, cholecystitis, choledocholithiasis, and cholangitis—were identified by ICD-10 codes. Propensity score matching (1:1 greedy nearest neighbor; caliper 0.1 SD) balanced demographics, comorbidities, GI surgeries, and antidiabetic medications. Results: After propensity score matching, 32,052 patients were included (16,026 per cohort), achieving excellent covariate balance with standardized mean differences < 0.1 for nearly all variables. GLP-1/GIP agonist use was associated with significantly lower risks of multiple biliary complications. Cholelithiasis occurred in 3.5% of GLP-1/GIP users compared with 6.3% of nonusers (risk ratio [RR] 1.81, 95% CI 1.64–2.00; hazard ratio [HR] 1.27, 95% CI 1.14–1.41; p < 0.001). Cholecystitis similarly occurred less frequently among users (0.8% vs. 2.2%; RR 2.74, 95% CI 2.24–3.34; HR 1.85, 95% CI 1.50–2.27; p < 0.001). Choledocholithiasis was also reduced in the GLP-1/GIP cohort (0.6% vs. 1.5%; RR 2.72, 95% CI 2.14–3.46; HR 1.90, 95% CI 1.48–2.44; p < 0.001). Cholangitis events were rare in both groups (0.1% vs. 0.2%) with no significant difference on survival analysis (HR 1.07, 95% CI 0.58–1.97; p = 0.08). Conclusions: In adults with T2DM and IBD, GLP-1 and dual GLP-1/GIP receptor agonists are associated with substantially reduced risks of gallstone-related complications. These real-world data support the gastrointestinal safety of GLP-1–based therapy in a high-risk population and suggest possible biliary protective effects warranting prospective, agent-specific studies. Full article

The limited efficacy of cytotoxic chemotherapy in the context of gastric cancer treatment is largely driven by profound molecular and biological heterogeneity. In contrast, the development of antibody-mediated therapies has ushered in a new era of precision oncology by enabling selective molecular targeting and immune modulation. This review includes a comprehensive overview of the evolution of antibody-based therapeutics in gastric cancer, highlighting early breakthroughs, subsequent setbacks, and recent advances that have reshaped the treatment landscape. We summarize the current standard regimens targeting HER2, VEGFR2, PD-1/PD-L1, and CLDN18.2 and examine pivotal clinical trials evaluating monoclonal antibodies directed against these pathways. We also discuss emerging therapeutic modalities, including next-generation antibody–drug conjugates (ADCs), bispecific antibodies, and chimeric antigen receptor (CAR) T-cell therapies. Trastuzumab first established HER2-targeted therapy in gastric cancer, but the failure of trastuzumab emtansine (T-DM1) led to a decade-long stagnation until the advent of trastuzumab deruxtecan (T-DXd), which demonstrated robust clinical activity and defined a new standard of care. While bevacizumab failed to improve survival, the anti-VEGFR2 antibody ramucirumab emerged as an effective second-line therapy. Immune checkpoint inhibitors, including nivolumab and pembrolizumab, have been incorporated into first-line treatment for PD-L1-positive disease based on landmark trials such as CheckMate 649 and KEYNOTE-811. More recently, the CLDN18.2-targeted antibody zolbetuximab has expanded therapeutic options for biomarker-selected patients. Concurrently, a diverse pipeline of immune-based strategies—such as TROP2-directed ADCs, bispecific antibodies, and CAR-T cell therapies—is undergoing active clinical development. Together, advances in biomarker-driven antibody therapeutics are accelerating personalized cancer care and improving clinical outcomes in patients with gastric cancer. Full article

Background: Malnutrition is a prevalent and under-recognized condition in patients with type 2 diabetes mellitus (T2DM), contributing to various complications, including liver fibrosis. In this study, we aimed to evaluate the association between malnutrition and liver fibrosis in patients with T2DM, and to assess whether inflammation mediates this relationship. Methods: In this prospective single-centre study, 87 adult outpatients with T2DM underwent nutritional assessment using the Subjective Global Assessment (SGA) and liver stiffness measurement by transient elastography. Metabolic dysfunction-associated steatotic liver disease (MASLD) was diagnosed according to EASL guidelines. C-reactive protein (CRP) was measured as a marker of systemic inflammation. Multivariable linear regression and mediation analysis were performed, adjusting for age and sex. Results: Malnutrition was present in 50.6% of patients, MASLD in 66.7%, and both conditions coexisted in 36.8%. Malnutrition (B = 2.29, p < 0.001), MASLD (B = 1.54, p = 0.001), smoking (B = 1.06, p = 0.014), and CRP (B = 0.32, p < 0.001) were independently associated with increased liver stiffness. CRP partially mediated the effect of malnutrition on liver stiffness (indirect effect = 0.54; 95% CI 0.20–0.95), accounting for 18% of the total effect. Conclusions: In T2DM, malnutrition is a strong independent predictor of liver fibrosis, with its effect partially mediated by systemic inflammation. Addressing nutritional status and inflammatory burden may help slow fibrotic progression in this high-risk population. Full article

Background: Advanced hybrid closed-loop (aHCL) systems have improved glycemic control in individuals with type 1 diabetes (T1DM). However, it remains unclear whether their efficacy and safety differ by patient’s sex, in view of known sex-related physiological and behavioral differences in disease control and management. Methods: This retrospective, single-center study included 176 adults with T1DM starting aHCL therapy with Medtronic MiniMed™ 780G. Continuous glucose monitoring (CGM) metrics, glycated hemoglobin (HbA1c), and glycemic variability (GV) indexes were collected at baseline, 6 months, and 12 months after starting aHCL therapy. Only patients with at least 70% sensor usage were included at each time point. The primary outcome was the assessment of sex-related differences in CGM metrics at 12 months. Secondary outcomes included changes in HbA1c and GV indexes by sex and over time. Results: TIR increased significantly at 6 (+6.6%, p < 0.001) and 12 months (+5.4%, p < 0.001), TAR decreased, and TBR remained stable. HbA1c was significantly reduced at both 6 and 12 months (−0.6%, p < 0.001). Improvements were consistent in both males and females, with females exhibiting better improvement in HbA1c compared to males (−0.4%, p = 0.049). No significant sex differences were found in CGM metrics at 12 months. GV indexes improved significantly in both groups, regardless of sex. At the multivariable analysis, only HbA1c <7.0% at baseline was associated with the achievement of the composite outcome (TIR > 70%, TBR < 4%, HbA1c < 7.0%). Conclusions: aHCL therapy improved glycemic control and GV in adults with T1DM, regardless of the patient’s sex. These results support the generalizability of aHCL therapy and underscore the need to ensure equitable access to technologies rather than sex-specific adjustments. Full article

Metabolic dysfunction–associated fatty liver disease (MASLD) is associated with severe forms of liver injury, including fibrosis and cirrhosis. The main risk factors for MASLD—obesity, type 2 diabetes mellitus (T2DM), dyslipidemia, and insulin resistance (IR)—contribute to metabolic disturbances that initiate hepatic steatosis. Metabolic and alcohol-related liver disease (MetALD) describes patients with MASLD who also present alcohol-associated hepatic injury. Chronic oxidative and inflammatory stress promotes the progression of steatosis in both conditions. T2DM and chronic alcohol consumption are independent lifestyle-related risk factors for cirrhosis within the spectrum of metabolic dysfunction–related liver disease (MASLD and MetALD). The coexistence of both conditions may exacerbate hepatic pathological alterations. IR, which is frequently observed in patients with cirrhosis, can lead to the development of a condition known as hepatogenic diabetes (HD). HD is characterized by hyperinsulinemia, IR, and β-cell dysfunction occurring during the onset of cirrhosis and is associated with hepatic inflammation even in the absence of traditional metabolic risk factors such as obesity or a prior history of T2DM. In this context, alcohol intake enhances lipolysis in peripheral tissues, promotes hepatic steatosis, and aggravates metabolic dysfunction, ultimately contributing to excessive mitochondrial production of reactive oxygen species (ROS). Therefore, the present review examines the role of oxidative stress—both alcohol-related and non-alcohol–related—in the pathogenesis of HD, with particular emphasis on ethanol metabolism, oxidative stress, and their interactions in conditions such as T2DM and MetALD. Full article

Background: Type 2 diabetes mellitus (T2DM) remains one of the most significant public health problems, and its incidence rate is steadily increasing worldwide despite scientific and technological progress in the field of medicine. The focus of research in this area is gradually shifting from classic risk factors—such as obesity, sedentary lifestyle and genetic predisposition—toward additional, potentially modifiable contributors such as micronutrient imbalances; among them are disturbances in zinc homeostasis that may influence glucose metabolism and oxidative stress. Objective: This systematic review with narrative synthesis aims to examine the bidirectional relationship between zinc status and T2DM and to evaluate whether zinc screening and personalized nutritional support could contribute to comprehensive metabolic management. Methods: A literature search was conducted in the PubMed database and the Cochrane library for studies published between 2010 and 2024. Studies assessing zinc status or supplementation in relation to the risk, progression, or management of T2DM were included. Data were synthesized narratively, focusing on clinical and mechanistic evidence. Results: Thirty studies met the inclusion criteria. Evidence indicates that zinc imbalance (both deficiency and excess) is associated with T2DM risk and outcomes. Zinc deficiency may impair insulin synthesis and signaling, promote oxidative stress and inflammation, while excessive zinc intake may induce metabolic disturbances. T2DM itself may lead to reduced zinc status via altered absorption and increased excretion. While some studies suggest modest improvements in glycemic or lipid parameters following zinc supplementation, findings remain inconsistent and context-dependent. The prevalence of suboptimal zinc status in certain populations supports the rationale for targeted screening rather than routine supplementation. Conclusions: Zinc is mechanistically involved in insulin synthesis, antioxidant defense, and inflammation control, but current clinical evidence does not justify its use as a therapeutic agent in T2DM. Instead, assessment of zinc status and individualized correction of deficiency may represent a component of personalized nutritional support, particularly for patients with long disease duration, poor dietary quality, or genetic predispositions affecting zinc metabolism. Full article

Breast cancer is the most common cancer and the most important cause of cancer-related death in females worldwide. Antibody–drug conjugates (ADCs) represent a novel class of targeted therapies that combine the precision of monoclonal antibodies with the potent cell-killing activity of cytotoxic drugs. This review highlights recent mechanistic, technological, and clinical developments of ADCs in breast cancer, including next-generation ADCs beyond those that target HER2 (human epidermal growth factor receptor 2). Authors performed a systematic literature study for ADCs and their structural features, including their components (antibody, linker, and payload) and their therapeutic efficacy. A frame of preclinical research findings and clinical evidence integration of HER2-targeted therapy outcomes in HER2-positive, HER2-low, and triple-negative breast cancer (TNBC) subtypes were presented. Clinical studies of antibody–drug conjugates such as trastuzumab emtansine (T-DM1), trastuzumab deruxtecan (T-DXd), and sacituzumab govitecan have demonstrated significant improvements in progression-free survival and overall survival across diverse breast cancer patient populations. ADCs offer unique advantages in breast cancer therapy by combining the precision of targeted antibodies with the potency of chemotherapy drugs. This allows them to selectively kill cancer cells, overcome resistance, reduce toxicity to healthy tissues, and expand treatment options for difficult subtypes like HER2-low and triple-negative breast cancer. Unlike previous reviews focusing on HER2-targeted ADCs, herein we review exciting ADCs targeting HER3 HER3 (human epidermal growth factor receptor 3) and Nectin-4, as well as the implications of bispecific and immune-stimulatory ADCs in the clinic. Additionally, it features mechanism-based innovations and novel trial data that revolutionize ADC applications in the HER2-low as well as the triple-negative breast cancer subtypes. The advent of ADC is changing precision oncology in breast cancer. With a new design and indications evolving, they are an attractive avenue for bypassing resistance and reducing toxicity and ultimately improving patient outcomes in the molecular subtypes. The present review summarizes recent advancements in antibody–drug conjugates (ADCs) and emerging targeted therapeutic strategies for breast cancer. It covers mechanistic insights, linker–payload innovations, receptor-based targeting approaches, clinical trial progress, and next-generation modalities that extend beyond HER2-directed ADCs. Current challenges, safety profiles, and future opportunities in engineering more selective and effective ADC platforms are also discussed. Full article

Background/Objectives: Self-care is essential in managing type 2 diabetes (T2DM), yet it remains suboptimal among patients. This systematic review aimed to determine whether self-regulation-based self-management interventions improve glycemic control, self-efficacy, and quality of life among adults with type 2 diabetes mellitus (T2DM), including individual and family-based approaches. Methods: Four major databases (Scopus, ScienceDirect, ProQuest, and PubMed) were systematically searched for English-language studies following PRISMA guidelines. Screening was performed using Rayyan, and study quality was assessed with the JBI critical appraisal tool. Data were synthesized based on PICO outcomes and study design to identify key patterns. The review was registered in PROSPERO (CRD42024594398). Results: A total of 881 articles were identified, and 31 met the inclusion criteria. Most studies were randomized controlled trials (54.8%), with diabetes self-management education (DSME) being the most common intervention (41.9%), followed by self-regulation training (12.9%). Nearly half of the studies measured blood glucose and quality-of-life outcomes (22.6%), while others focused on knowledge, behavior, and self-efficacy (19.4%). Only a few studies addressed individual and family-oriented interventions. Conclusions: DSME and self-regulation-based approaches are recommended as complementary strategies to improve diabetes self-management. This review introduces a novel integrative model linking disease interpretation, coping strategies, and family support, and highlights their influence on patient self-care behaviors. Future research should empirically test this model to clarify the dynamic interactions among its domains and their effects on glycemic control and health outcomes. Full article

Background: Type 2 diabetes mellitus (T2DM) is increasingly recognized as affecting not only the retina but also the ocular surface. Chronic hyperglycemia can disrupt meibomian gland function, reduce tear secretion, and impair corneal sensitivity, leading to tear film instability and symptoms of dry eye disease. However, previous studies have reported variable findings, and the extent of these alterations remains uncertain. Methods: Following PRISMA guidelines, this systematic review and meta-analysis evaluated observational studies that compared tear film parameters between adults with T2DM and non-diabetic controls. Eligible studies assessed one or more of the following: invasive or non-invasive tear break-up time, Schirmer test, tear meniscus height, or Ocular Surface Disease Index (OSDI). Results: Twenty-four studies involving approximately 3500 eyes were included. Most reported significantly reduced tear stability and secretion in diabetic participants compared with controls. Tear break-up times were consistently shorter in T2DM, indicating a less stable tear film. Schirmer test results demonstrated lower tear production correlated with diabetes duration and poor glycemic control. Tear meniscus height was modestly reduced in T2DM, reflecting decreased tear reservoir volume. Subjective symptoms, as measured by OSDI, were generally higher among patients with T2DM, suggesting greater ocular surface discomfort. Conclusions: T2DM is strongly associated with tear film instability, reduced tear secretion, and increased dry eye symptoms. These findings suggest that diabetic care should include routine ocular surface assessment and highlight the need for standardized, longitudinal investigations. Full article

Background and Objectives: There is no universal agreement with regard to the correlation between Helicobacter pylori (H. pylori) infection, type 2 diabetes mellitus (T2DM), and ABO blood group antigens. The data related to these are limited. The purpose of this study is to explore the correlation and frequency of H. pylori infection with T2DM and ABO blood group of adults that reside in Jordan. Materials and Methods: This study adopts a cross-sectional comparison of 149 patients diagnosed with T2DM and 168 non-diabetic controls. The One-Step Immunochromatographic DiaSpot^® test was used to diagnose H. pylori, while standardized hemagglutination through the use of monoclonal anti-A, anti-B, and anti-D reagents was used for ABO blood grouping. Analyses were conducted on the correlation between H. pylori infection, diabetes, and ABO blood group through logistic regression. Results: A total of 89 out of the 317 participants tested positive for H. pylori infection (overall seroprevalence = 28.0%), consisting of 51 of the 149 T2DM patients (34.2%) and 38 (22.6%) of the 168 non-diabetic controls. A significant association was observed between diabetes status and H. pylori infection (χ²(1) = 4.71, p < 0.05), with the probability of being H. pylori-positive 1.78 times higher among diabetics (95% CI: 1.085–2.921). A significant association was found between blood group and H. pylori infection, (χ²(3), n = 317) = 15.01, p < 0.001. Of the 89 H. pylori-positive patients, 21 (23.6%) were in blood group A, 13 (14.6%) in group B, and 44 (49.4%) in group O, with the remaining 11 (12.4%) patients in blood group AB. Conclusions: Significant associations were found between H. pylori infection and both T2DM and blood type. Further longitudinal studies that include larger, more diverse populations and more potentially significant factors are needed to clarify these relationships. Full article